Highlights Human MSCs are free from SARS-CoV-2 infection. Human MSCs have no risk of assisting SARS-CoV-2 infection in other cells. Implanted human MSCs are unable to up-regulate the expression of ACE2 and TMPRSS2 in the lung tissues of mice under different inflammatory challenge conditions.
In this study, we propose a blockchain-based privacy-preserving vaccine passport system for the global prevention and control of infectious diseases. The system operates a double-chain framework which consists of a public blockchain and a consortium blockchain. Among them, the combination of the immutability of the public blockchain and Internet of Things (IoT) technology in the supply chain ensures the openness and transparency of the cold chain logistics records of the vaccines covering the stages from auditing to the target vaccination hospitals. The system adopts the consortium blockchain to achieve the balance between the protection of users’ vaccination privacy and auditing by the government departments. Specifically, a distributed system-based threshold signature is adopted in the vaccine qualification phase to resist collusion between the vaccine manufacturing company and vaccine approval institutions. The cryptographic tools such as the anonymous credentials, zero-knowledge protocols, and range proofs ensure that users do not disclose any private information other than proving that they have a legally valid vaccine passport when users display the vaccine passports to customs. At the same time, customs can apply various vaccine prevention policies based on the conditions on the specific vaccine passports. Regarding the security properties of the system, a formal security model is given along with the corresponding security proofs.
Background: Cancer stem cells (CSC) carry out a vital responsibility throughout the entire progress of colorectal cancer (CRC), and fulfil an essential biological function. However, lncRNAs participate in regulating CRC stem cells (CCSCs) and correlate strongly with the patients' prognosis. Therefore, it is crucial to identify the CCRC-related lncRNAs in CRC. Methods: We identified CCRCs-related lncRNAs through the Cell marker and TCGA databases. And the CCSC-related lncRNAs model was constructed by the differential, cox survival , and lasso regression analysis. Combining the GEO dataset, we determined the prognostic value by Kaplan-Meier analysis, univariate and multivariate cox survival analysis. Moreover, principal component analysis (PCA), clinical characterization, nomogram, gene mutation, gene set enrichment analysis (GSEA), immune microenvironment (TME), chemotherapy, intergroup differential gene, and protein-protein interaction (PPI) analysis were conducted to analyze the risk model. Furthermore, the core genes in the sub-module were comprehensively characterized. Results: In this research, abnormally expressed, prognostic and CSC-related lncRNAs were firstly identified. Through the lasso regression model, we obtained a robust risk signature consisting of 4 CCSC-related lncRNAs (ZEB1-AS1,LINC00174,FENDRR and ALMS1-IT1). Then, the risk model was confirmed applicable in both TCGA and GEO cohorts. Further verification, the signature can be verified as a independent prognostic factor for CRC. Based on the CCSC-related lncRNA model, the high- and low-risk groups exhibited different stemness statuses, including gene expression, mutation status, signaling pathways, TME and chemotherapy response. The HOX family and HOX4 were centrally located in the PPI interaction and had an influential contribution in CRC. Conclusions: We established a 4 CCSC-related lncRNA signature with a promising prognosis. And the signature can appropriately estimate the gene mutation, TME, and chemotherapy outcomes for CRC patients. Furthermore, the CCSC-related lncRNAs and HOX4 can serve as noble biomarkers and promote the management of therapy clinically.
Histone deacetylases 1 (HDAC1), an enzyme that functions to remove acetyl molecules from ε-NH3 groups of lysine in histones, eliminates the histone acetylation at the promoter regions of tumor suppressor genes to block their expression during tumorigenesis. However, it remains unclear why HDAC1 fails to impair oncogene expression. Here we report that HDAC1 is unable to occupy at the promoters of oncogenes but maintains its occupancy with the tumor suppressors due to its interaction with CREPT (cell cycle-related and expression-elevated protein in tumor, also named RPRD1B), an oncoprotein highly expressed in tumors. We observed that CREPT competed with HDAC1 for binding to oncogene (such as CCND1, CLDN1, VEGFA, PPARD and BMP4) promoters but not the tumor suppressor gene (such as p21 and p27) promoters by a chromatin immunoprecipitation (ChIP) qPCR experiment. Using immunoprecipitation experiments, we deciphered that CREPT specifically occupied at the oncogene promoter via TCF4, a transcription factor activated by Wnt signaling. In addition, we performed a real-time quantitative PCR (qRT-PCR) analysis on cells that stably over-expressed CREPT and/or HDAC1, and we propose that HDAC1 inhibits CREPT to activate oncogene expression under Wnt signaling activation. Our findings revealed that HDAC1 functions differentially on tumor suppressors and oncogenes due to its interaction with the oncoprotein CREPT.
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